Low Socioeconomic Status is Associated With Higher In-Hospital Mortality in Stanford Type a Aortic Dissection Repair: A Population Study of National Inpatient Sample From 2015 to 2020.

INTRODUCTION: Stanford Type A Aortic Dissection (TAAD) is characterized by a high in-hospital mortality rate and necessitates urgent surgical intervention. While socioeconomic status is known to influence health-care outcomes, its specific association with TAAD remains underexplored. This study aimed to investigate the population-based association between socioeconomic status with TAAD repair outcomes using a national registry. METHODS: Patients who had TAAD repair were identified in National Inpatient Sample from Q4 2015-2020. National Inpatient Sample stratified estimated median household income of residents within a patient's ZIP code. Patients residing in neighborhoods of incomes in the lowest and highest quartiles were selected as the study cohorts. Multivariable logistic regressions were used to compare in-hospital outcomes, adjusted for demographics, comorbid conditions, hospital characteristics, primary payer status, and transfer status. RESULTS: Compared to patients from high-income neighborhoods, patients in low-income communities had higher risks of mortality (adjusted odds ratio [aOR] 1.45, P = 0.01), acute kidney injury (aOR 1.225, P = 0.03), and infection (aOR 1.474, P = 0.02), as well as longer wait from admission to operation (24.96 ± 2.64 versus 18.00 ± 1.92 h, P = 0.03) and longer length of stay (15.06 ± 0.38 versus 13.80 ± 0.36 d, P = 0.01). In contrast, patients from low-income communities had less risk of hemorrhage/hematoma (aOR 0.691, P < 0.01) and lower total hospital charge (428,746 ± 10,658 versus 487,017 ± 16,770 US dollars, P < 0.01). CONCLUSIONS: Evidence suggests patients from lower-income communities may have limited access to health care and treatment delays, leading to higher mortality and complications. The underlying reasons for these disparities in economically disadvantaged communities warrant further investigation, which could focus on health-care accessibility, timely detection of TAAD, and prompt transfers to specialized centers.

Female patients have higher in-hospital mortality after type A aortic dissection repair: A population study from the national inpatient sample.

BACKGROUND: Stanford Type A Aortic Dissection (TAAD) is an emergent condition with high in-hospital mortality. Gender disparity in TAAD has been a topic of ongoing debate. This study aimed to conduct a population-based examination of gender disparities in short-term TAAD outcomes using the National/Nationwide Inpatient Sample (NIS) database, the largest all-payer database in the US. METHODS: Patients undergoing TAAD repair were identified in NIS from the last quarter of 2015-2020. Multivariable logistic regressions were used to compare in-hospital outcomes between male and female patients, adjusted for demographics, comorbidities, hospital characteristics, primary payer status, and transfer status. RESULTS: There were 1454 female and 2828 male patients identified who underwent TAAD repair. Female patients presented with TAAD were at a more advanced mean age (64.03 ± 13.81 vs. 58.28 ± 13.43 years, p < 0.01) and had greater comorbid burden. Compared to male patients, female patients had higher risks of in-hospital mortality (17.88% vs. 13.68%, adjusted odds ratio (aOR) = 1.266, p = 0.01). In addition, female patients had higher pericardial complications (20.29% vs. 17.22%, aOR = 1.227, p = 0.02), but lower acute kidney injury (AKI; 39.96% vs. 53.47%, aOR = 0.476, p < 0.01) and venous thromboembolism (VTE; 1.38% vs. 2.65%, aOR = 0.517, p = 0.01). Female patients had comparable time from admission to operation and transfer-in status, longer hospital stays, but fewer total hospital expenses. CONCLUSION: Female patients were 1.27 times as likely to die in-hospital after TAAD repair but had less AKI and VTE. While there is no evidence suggesting delay in TAAD repair for female patients, the disparities might stem from other differences such as in care provided or intrinsic physiological variations.

Patients with alcohol abuse have higher risks of complications after coronary artery bypass grafting: a population-based study of National Inpatient Sample from 2015 to 2020.

BACKGROUND: Alcohol abuse (AA) has s high prevalence, affecting 10 to 15 million Americans. While AA was demonstrated to negatively impact cardiovascular health, limited evidence from existing studies presents conflicting findings regarding the effects of AA on coronary artery bypass grafting (CABG) outcomes. This study aimed to compare the in-hospital outcomes after CABG between AA and non-AA patients. METHODS: Patients who underwent CABG were identified in National Inpatient Sample from Q4 2015-2020. Exclusion criteria included age<18 years and concomitant procedures. A 1:3 propensity-score matching was used to address differences in demographics, socioeconomic status, primary payer status, hospital characteristics, comorbidities, and transfer/admission status between AA and non-AA patients. In-hospital outcomes after CABG were examined. RESULTS: There were 5,694 (3.39%) AA patients who underwent CABG. After matching, 17,315 from 162,488 non-AA patients were matched to all AA patients. AA and non-AA patients had comparable mortality (1.64% vs 1.55%, p=0.67) and MACE (2.46% vs 2.56%, p=0.73). However, AA patients had higher cardiogenic shock (8.31% vs 7.43%, p=0.03), mechanical ventilation (11.51% vs 7.96%, p<0.01), hemorrhage/hematoma (57.49% vs 54.75%, p<0.01), superficial (0.99% vs 0.61%, p<0.01) and deep wound complications (0.37% vs 0.18%, p=0.02), reopen surgery for bleeding control (0.92% vs 0.63%, p=0.03), transfer out (21.00% vs 16.38%, p<0.01), longer time from admission to operation (p<0.01), longer length of stay (p<0.01), and higher hospital charge (p<0.01). CONCLUSION: While AA was not found to be linked with in-hospital mortality or MACE after CABG, it was independently associated with postoperative complications. These findings could enhance preoperative risk stratification for AA patients and inform postoperative management following CABG.

Socioeconomic disparity in transcatheter and surgical aortic valve replacement: a population study of National Inpatient Sample from 2015 to 2020.

There is limited data on the effect of socioeconomic status (SES) on transcatheter (TAVR) and surgical aortic valve replacement (SAVR) outcomes for aortic stenosis (AS). This study conducted a population-based analysis to assess the influence of SES on valve replacement outcomes. Patients with AS undergoing TAVR or SAVR were identified in National Inpatient Sample from Q4 2015-2020. Multivariable logistic regressions were used to compare in-hospital outcomes between patients living in neighborhoods of income at the lowest and highest quartiles. Of 613,785 AS patients, 9.77% underwent TAVR and 10.13% had SAVR. These rates decline with lower neighborhood income levels, with TAVR/SAVR ratio also declining in lower-income areas. Excluding concomitant procedures, 58,064 patients received isolated TAVR (12,355 low-income and 15,212 high-income) and 43,694 underwent isolated SAVR (10,029 low-income and 10,811 high-income). Low-income patients, in both TAVR and SAVR, were younger but had more comorbid burden. For isolated TAVR, outcomes were similar across income groups. However, for isolated SAVR, low-income patients experienced higher in-hospital mortality (aOR = 1.44, p < 0.01), pulmonary (aOR = 1.13, p = 0.01), and renal complications (aOR = 1.14, p < 0.01). They also had more transfers, longer waits for operations, and extended hospital stays. Lower-income communities had reduced access to TAVR and SAVR, with TAVR accessibility being particularly limited. When given access to TAVR, patients from lower-income neighborhoods had mostly comparable outcomes. However, patients from low-income communities faced worse outcomes in SAVR, possibly due to delays in treatment. Ensuring equitable specialized healthcare resources including expanding TAVR access in economically disadvantaged communities is crucial.

In-hospital outcome of type A aortic dissection repair in patients with chronic obstructive pulmonary disease: A population study of National Inpatient Sample from 2015 to 2020.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common comorbidity that has been linked to higher mortality and respiratory complications in cardiac surgery. However, the postoperative outcomes for COPD patients undergoing Type A Aortic Dissection (TAAD) repair remain unexplored. Thus, this study aimed to assess the impact of COPD on in-hospital outcomes of TAAD repair in a national registry. METHODS: Patients undergoing TAAD repair were identified in National Inpatient Sample from the last quarter of 2015-2020. Multivariable logistic regressions were used to compare in-hospital outcomes between patients with and without COPD, where demographics, comorbidities, hospital characteristics, primary payer status, and transfer status were adjusted. RESULTS: There were 701 (16.37 %) COPD patients and 3581 (83.63 %) non-COPD patients who went under TAAD repair, where the prevalence of COPD was higher than in the general population (6 %). COPD and non-COPD patients have comparable rates of in-hospital mortality (14.69 % vs 15.19 %, aOR 1.016, 95 CI 0.797-1.295, p = 0.9) and there was no indication of delayed surgery. However, COPD patients had a higher risk of mechanical ventilation (37.80 % vs 31.42 %, aOR 1.521, 95 CI 1.267-1.825, p < 0.01) and a higher rate of transferring out to other facilities (38.37 % vs 32.23 %, aOR 1.271, 95 CI 1.054-1.533, p = 0.01). In addition, COPD patients had a longer hospital length of stay (14.28 ± 11.32 vs 13.85 ± 12.78 days, F = 5.61, p = 0.01). CONCLUSION: The presence of COPD could be a risk factor for the development of aortic dissection. However, outcomes for COPD patients were largely similar to those without COPD. These findings can be valuable for preoperative assessments and tailoring perioperative care for COPD patients undergoing TAAD repair.

Coronary artery bypass grafting outcomes of patients with human immunodeficiency virus: a population-based study of National Inpatient Sample from 2015 to 2020.

Individuals affected by human immunodeficiency virus (HIV) have a growing demand for coronary artery bypass grafting (CABG) due to heightened risk for cardiovascular diseases and extended life expectancy. However, CABG outcomes in HIV patients are not well-established, with insights only from small case series studies. This study conducted a comprehensive, population-based examination of in-hospital CABG outcomes in HIV patients. Patients underwent CABG were identified in National Inpatient Sample from Q4 2015-2020. Patients with age < 18 years and concomitant procedures were excluded. A 1:5 propensity-score matching was used to address preoperative group differences. Among patients who underwent CABG, 613 (0.36%) had HIV and were matched to 3119 out of 167,569 non-HIV patients. For selected HIV patients, CABG is relatively safe, presenting largely similar outcomes. After matching, HIV and non-HIV patients had comparable in-hospital mortality rates (2.13% vs. 1.67%, p = 0.40). Risk factors associated with mortality among HIV patients included previous CABG (aOR = 14.32, p = 0.01), chronic pulmonary disease (aOR = 8.24, p < 0.01), advanced renal failure (aOR = 7.49, p = 0.01), and peripheral vascular disease (aOR = 6.92, p = 0.01), which can be used for preoperative risk stratification. While HIV patients had higher acute kidney injury (AKI; 26.77% vs. 21.77%, p = 0.01) and infection (8.21% vs. 4.18%, p < 0.01), other complications were comparable between the groups.

Regional remodeling strain and its association with myocardial apoptosis after myocardial infarction in an ovine model.

OBJECTIVE: Progressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling. METHODS: Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins. RESULTS: At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 +/- 0.1 mm Hg, a decrease in ejection fraction from 54.19% +/- 5.68% to 30.55% +/- 2.72%, and an end-diastolic volume increase of 46.08 +/- 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.27, P < .05), caspase-3 (r(2) = 0.31, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.28, P < .05), caspase-3 (r(2) = 0.43, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.37, P < .05). CONCLUSION: Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.

Early in vivo experience with the pediatric Jarvik 2000 heart.

The need for smaller, more efficient ventricular assist devices that can be used in a more chronic setting have led to exploration of mechanical circulatory support in the pediatric population. The pediatric Jarvik 2000 heart (child size), under development, was implanted in six juvenile sheep and studied for both acute fit and chronic performance evaluation. Daily hemodynamic measurements of cardiac output and pump output at varying pump speeds were taken. In addition, plasma free hemoglobin, lactic acid dehydrogenase, and platelet activation from blood samples were determined at baseline, after implantation, and twice a week thereafter. The measured flow through the outflow graft at increasing speeds from 10,000 rpm to 14,000 rpm with an increment of 1,000 rpm were 1.47 +/- 0.43, 1.89 +/- 0.52, 2.36 +/- 0.61, 2.80 +/- 0.73, and 3.11 +/- 0.86 (L/min). The baseline plasma free hemoglobin was 11.95 +/- 4.76 (mg/dL), with subsequent mean values being <30 mg/dL at postimplantation and weekly postimplantation measurements. Both lactic acid dehydrogenase and platelet activation showed an acute increase within the first week after implantation with subsequent return to baseline by 2 weeks after surgery. Our initial animal in vivo experience with the pediatric Jarvik 2000 heart shows that a small axial flow pump can provide partial to nearly complete circulatory support with minimal adverse effects on blood components.

Strain-related regional alterations of calcium-handling proteins in myocardial remodeling.

BACKGROUND: Cardiac remodeling has been shown to have deleterious effects at both the global and local levels. The objective of this study is to investigate the role of strain in the initiation of structural and functional changes of myocardial tissue and its relation to alteration of calcium-handling proteins during cardiac remodeling after myocardial infarction. METHODS: Sixteen sonomicrometry transducers were placed in the left ventricular free wall of 9 sheep to measure the regional strain in the infarct, adjacent, and remote myocardial regions. Hemodynamic, echocardiographic, and sonomicrometry data were collected before myocardial infarction, after infarction, and 2, 6, and 8 weeks after infarction. Regional myocardial tissues were collected for calcium-handling proteins at the end study. RESULTS: At time of termination, end-systolic strains in 3 regionally distinct zones (remote, adjacent, and infarct) of myocardium were measured to be -14.65 +/- 1.13, -5.11 +/- 0.60 (P < or = .05), and 0.92 +/- 0.56 (P < or = .05), respectively. The regional end-systolic strain correlated strongly with the abundance of 2 major calcium-handling proteins: sarcoplasmic reticulum Ca2+ adenosine triphosphatase subtype 2a (r2 = 0.68, P < or = .05) and phospholamban (r2 = 0.50, P < or = .05). A lesser degree of correlation was observed between the systolic strain and the abundance of sodium/calcium exchanger type 1 protein (r2 = 0.17, P < or = .05). CONCLUSIONS: Regional strain differences can be defined in the different myocardial regions during postinfarction cardiac remodeling. These differences in regional strain drive regionally distinct alterations in calcium-handling protein expression.

Optimizing donor heart outcome after prolonged storage with endothelial function analysis and continuous perfusion.

BACKGROUND: By minimizing tissue ischemia, continuous perfusion (CP) during organ transport may increase the safety of "marginal donors." My colleagues and I investigated whether an analysis of donor heart viability predicts recovery of grafts challenged with a 24-hour preservation interval. METHODS: Dog hearts underwent cold static storage (CS) for 8 hours (n = 8) or 24 hours (n = 2) or CP for 24 hours with cold asanguinous, oxygenated solution (n = 8). Myocardial systolic and diastolic function and oxygen and lactate consumption were assessed at base line, during CP, and after Langendorff blood reperfusion. Base line endothelial function was evaluated by the percentage transcoronary change ([coronary sinus - aorta]/aorta) in myeloperoxidase and by platelet function and coronary flow reserve after 20 seconds of coronary artery occlusion. During CP, the endothelium was assessed by transcoronary protein release and coronary resistance. Edema was assessed by weight gain and histology. RESULTS: Base line systolic and metabolic functions showed no relation to post-Langendorff function. Compared with CS, CP resulted in a greater recovery in systolic function (87% +/- 35% vs 65% +/- 15% of baseline; p = 0.05) and a shorter interval required for lactate consumption to exceed production (7.0 +/- 6.8 minutes vs 15.0 +/- 8.9 minutes; p = 0.06). Endothelial function was heterogeneous: coronary flow reserve, 2.7 +/- 0.7; percentage change in myeloperoxidase, -8.4% +/- 6.8%; and change in platelet function, 4.3% +/- 3.5%, as determined by thromboelastography angle at base line. Protein release during CP for 24 hours was 8.3 +/- 7.1 g. Two factors predicted more than 75% systolic pressure generation recovery: use of CP and normal endothelial function (p = 0.05; Fisher's exact test). However, CP led to edema according to histology, weight gain (72 +/- 29 g), and impaired diastolic function versus CS (end-diastolic pressure-volume relationship, 1.4 +/- 0.4 mm Hg/mL vs 0.8 +/- 0.3 mm Hg/mL; p = 0.08). CONCLUSIONS: Better systolic function despite 16 hours' more preservation than cold storage corroborates the idea that CP supports aerobic metabolism at physiologically important levels. Viability analysis focused on endothelial function and identified organs that were able to tolerate this 24-hour preservation interval.